ライフサイエンスコーパス: tumor invasion

1 synergy with androgen receptor in mediating tumor invasion.

2 lls rescued the aggressive 3D phenotypes and tumor invasion.

3 ous diseases such as cardiac hypertrophy and tumor invasion.

4 ceptor, which can promote cell migration and tumor invasion.

5 y correlated with histological parameters of tumor invasion.

6 mined the role of HNK-1 glycan in astrocytic tumor invasion.

7 Cartilage is resistant to tumor invasion.

8 yrosination occurs at the earliest stages of tumor invasion.

9 talloproteinases, which are known to promote tumor invasion.

10 utic target for prevention of EMT-associated tumor invasion.

11 itical for the initiation and progression of tumor invasion.

12 the epithelial phenotype and a suppressor of tumor invasion.

13 ding stromal collagen at the leading edge of tumor invasion.

14 volume and surface area but had no effect on tumor invasion.

15 olecular explanation of how Pdcd4 suppresses tumor invasion.

16 ing proteinases, that play critical roles in tumor invasion.

17 l-appreciated role in matrix degradation and tumor invasion.

18 low avidity for tumor Ag were inefficient in tumor invasion.

19 ne kinase promotes invadopodia formation for tumor invasion.

20 signal-induced activation of PIKE-A/Akt and tumor invasion.

21 g, tumor dissemination, cell co-culture, and tumor invasion.

22 BM remodeling occurs during development and tumor invasion.

23 ion of BM is essential for developmental and tumor invasion.

24 that inhibits neoplastic transformation and tumor invasion.

25 ession as new hallmarks of CAFs that promote tumor invasion.

26 ronan/CD44s signaling in underpinning breast tumor invasion.

27 by both TIMP and RECK are required to block tumor invasion.

28 lular structures that are thought to mediate tumor invasion.

29 nce of any one of these three genes impaired tumor invasion.

30 rity induces JNK-mediated cell migration and tumor invasion.

31 ugh disruption of cell growth, survival, and tumor invasion.

32 on of adherent cells during wound repair and tumor invasion.

33 s junctions contributes to cell motility and tumor invasion.

34 edded in collagen that provide a lattice for tumor invasion.

35 rate specificity in collagen proteolysis and tumor invasion.

36 lly explaining their differential effects on tumor invasion.

37 tions with the extracellular matrix regulate tumor invasion.

38 cytoskeleton remodeling, cell adhesion, and tumor invasion.

39 unclear how collagen organization influences tumor invasion.

40 of hypoxic stimulation that is important for tumor invasion.

41 ialylation likely plays a role in colorectal tumor invasion.

42 on between TbetaRII expression and length of tumor invasion.

43 nt is not limited to being a barrier against tumor invasion.

44 ta1 on pericellular collagen degradation and tumor invasion.

45 rovide insight into how TF may contribute to tumor invasion.

46 nderstanding development, wound healing, and tumor invasion.

47 r of cell motility, a necessary component of tumor invasion.

48 4 is often associated with morphogenesis and tumor invasion.

49 corresponded with the onset of seizures and tumor invasion.

50 ed MMP2, a secreted proteinase key for brain tumor invasion.

51 the degradation of extracellular matrix and tumor invasion.

52 umor microenvironment and is correlated with tumor invasion.

53 or of matrix metalloproteinase 2 (TIMP2) and tumor invasion.

54 ite and elicited leukocytic infiltration and tumor invasion.

55 al oncogenic signaling pathways that promote tumor invasion.

56 This leads, in turn, to decreased tumor invasion.

57 a, creating a microenvironment permissive to tumor invasion.

58 role of the tumor microenvironment in brain tumor invasion.

59 itically involved in HIF1alpha signaling and tumor invasion.

60 in HNSCC where they suppress invadopodia and tumor invasion.

61 igenesis, cancer cell survival and regulates tumor invasion.

62 and actin dynamics are modulated for EMT and tumor invasion.

63 EB1 sufficient for repression of miR-200 and tumor invasion.

64 plex and stimulates actin polymerization for tumor invasion.

65 ective treatment of choroid and ocular nerve tumor invasion (1 of 20 animals with invasive disease in

66 but increased significantly with submucosal tumor invasion (22%)[P = 0.0003].

67 5) versus a less invasive (worst pattern of tumor invasion 3) pattern of invasion, we identified a t

68 umors with a more invasive (worst pattern of tumor invasion 5) versus a less invasive (worst pattern

69 ed accelerated tumor development, aggressive tumor invasion and a decreased survival rate in Ctnnb1(L

70 t, constitutively active ALK5-T204D enhances tumor invasion and angiogenesis by stimulating expressio

71 mediators of our defense system, to promote tumor invasion and angiogenesis remain incompletely unde

72 itor of metalloproteinase-3, an inhibitor of tumor invasion and angiogenesis, is up-regulated in both

73 at3 in tumor cells has been shown to promote tumor invasion and angiogenesis.

74 hose aberrant expression are correlated with tumor invasion and angiogenesis.

75 ted receptor-1, PAR-1) plays a major role in tumor invasion and contributes to the metastatic phenoty

76 ound angiogenic response leads to aggressive tumor invasion and destruction of surrounding brain tiss

77 ion of beta-catenin plays a critical role in tumor invasion and development.

78 Expression of kinase-inactive ALK5 reduces tumor invasion and formation of new blood vessels within

79 tion of key signaling pathways important for tumor invasion and growth.

80 ar adhesion, with potential implications for tumor invasion and keratinopathies, settings in which di

81 ntiated phenotype and showed increased local tumor invasion and lymph node metastasis.

82 otential role for TXAS-regulated pathways in tumor invasion and metastases and suggests that modulati

83 reased PTEN transcription, likely germane in tumor invasion and metastases but not initiation.

84 ged with various stresses and contributes to tumor invasion and metastases, whereas its deregulation

85 lial-Mesenchymal Transition (EMT) to promote tumor invasion and metastasis and can also inhibit apopt

86 It is widely believed to play a role in tumor invasion and metastasis and therefore to represent

87 Tumor invasion and metastasis are strongly regulated by

88 Tumor invasion and metastasis are the main causes of dea

89 nd angiogenic growth factors and facilitates tumor invasion and metastasis by degrading the ECM.

90 loproteinase-1 (MT1-MMP) plays a key role in tumor invasion and metastasis by degrading the extracell

91 TGF-beta promotes tumor invasion and metastasis by inducing an epithelial-

92 d survival, the roles of the PI3K pathway in tumor invasion and metastasis have not been well delinea

93 re associated with an increased frequency of tumor invasion and metastasis in certain cancers.

94 between angiopoietin 2 (Ang2) expression and tumor invasion and metastasis in various human cancers,

95 The process of tumor invasion and metastasis involves the destruction o

96 he standard form of CD44 in promoting breast tumor invasion and metastasis to the liver.

97 inding proteins that is directly involved in tumor invasion and metastasis via interactions with spec

98 Cholinergic-induced tumor invasion and metastasis were inhibited by pharmaco

99 pendent vessel normalization by CQ restrains tumor invasion and metastasis while improving chemothera

100 ion signature enriched for genes involved in tumor invasion and metastasis with patients experiencing

101 icroenvironment by stromal caveolin-1 favors tumor invasion and metastasis' by Goetz and colleagues,

102 Known to be vital for tumor invasion and metastasis, accumulating evidence als

103 trix by proteolytic enzymes is a hallmark of tumor invasion and metastasis, and aspartyl proteinase c

104 or receptors, molecules that are involved in tumor invasion and metastasis, and inactivation of criti

105 acellular matrix is an integral component of tumor invasion and metastasis, and much of this degradat

106 ased activity of SRC family kinases promotes tumor invasion and metastasis, and overexpression of the

107 actor (TGF)-beta(1) has been associated with tumor invasion and metastasis, and we have implicated cy

108 se transcriptase (hTERT) plays a key role in tumor invasion and metastasis, but the mechanism of its

109 an cancers and significantly correlated with tumor invasion and metastasis, but the mechanisms involv

110 MUC1 plays crucial roles in tumor invasion and metastasis, especially in opposing ce

111 t of beta-catenin and a key regulator during tumor invasion and metastasis, was also decreased.

112 ential mechanisms by which TF contributes to tumor invasion and metastasis, we investigated the effec

113 l transition (EMT) is an important driver of tumor invasion and metastasis, which causes many cancer

114 mplantation of mammary fibroblasts inhibited tumor invasion and metastasis, which was reversed by Tia

115 -9, which have been previously implicated in tumor invasion and metastasis.

116 atocyte growth factor c-Met, which can drive tumor invasion and metastasis.

117 clear factor kappaB signaling that represses tumor invasion and metastasis.

118 MDSCs infiltrate into tumors and promote tumor invasion and metastasis.

119 ily kinase (SFK) activity is associated with tumor invasion and metastasis.

120 ion through genes (i.e., TSP-1) important in tumor invasion and metastasis.

121 en postulated as an absolute requirement for tumor invasion and metastasis.

122 ht into the mechanism by which Ubc9 promotes tumor invasion and metastasis.

123 n, specifically their functions in mediating tumor invasion and metastasis.

124 induces functions that are also required for tumor invasion and metastasis.

125 Matrix degradation is a pivotal step in tumor invasion and metastasis.

126 lar hyperacetylated hsp90alpha may undermine tumor invasion and metastasis.

127 atrix metalloproteinase (MMP)-2, involved in tumor invasion and metastasis.

128 cell lines may be relevant to mechanisms of tumor invasion and metastasis.

129 erine proteases, which play crucial roles in tumor invasion and metastasis.

130 -RAS activates TGF-beta signaling to promote tumor invasion and metastasis.

131 the mechanisms by which telomerase promotes tumor invasion and metastasis.

132 ErbB2 (HER2, Neu) and Ras play key roles in tumor invasion and metastasis.

133 KLF6 and KLF6-SV1 can directly alter ovarian tumor invasion and metastasis.

134 e deregulated in many solid tumors and drive tumor invasion and metastasis.

135 skeletal development but also implicated in tumor invasion and metastasis.

136 ne of the few p53-targeted genes involved in tumor invasion and metastasis.

137 epithelial cells and influences HGF mediated tumor invasion and metastasis.

138 r matrix (ECM), which serves as a barrier to tumor invasion and metastasis.

139 pression in fibroblasts and hence facilitate tumor invasion and metastasis.

140 lar matrix degradation, an essential step in tumor invasion and metastasis.

141 , and it contributes to TNF-alpha-stimulated tumor invasion and metastasis.

142 as a potential therapeutic strategy against tumor invasion and metastasis.

143 vivo, inferring significance of legumain in tumor invasion and metastasis.

144 These processes have an established role in tumor invasion and metastasis.

145 romising therapeutic strategy for preventing tumor invasion and metastasis.

146 ial for primary tumor growth and facilitates tumor invasion and metastasis.

147 the EMT transcription factor ZEB1 to trigger tumor invasion and metastasis.

148 ng the roles of both TGF-beta and seprase in tumor invasion and metastasis.

149 opodia that have been uniquely implicated in tumor invasion and metastasis.

150 roteinase-2 (MMP-2) is a protease related to tumor invasion and metastasis.

151 n of miR-200, which is thought to facilitate tumor invasion and metastasis.

152 the potential to disrupt the role of FAP in tumor invasion and metastasis.

153 f EMT in cervical cancer and associated with tumor invasion and metastasis.

154 n about the underlying mechanisms that drive tumor invasion and metastasis.

155 We also found that some genes implicated in tumor invasion and metastatic behavior are epithelial ta

156 telomere length, which significantly reduced tumor invasion and metastatic potential.

157 expression on tumor cells has been linked to tumor invasion and metastatic spread, the contribution o

158 In the current work, tumor invasion and peritumoral pH were monitored over ti

159 ogen-independent impact of adipose tissue on tumor invasion and progression needs to be elucidated.

160 and resistance to apoptosis are hallmarks of tumor invasion and progression to metastatic disease, bu

161 ithin the epithelial microenvironment impact tumor invasion and progression.

162 at RNAi-mediated silencing of NEMO increased tumor invasion and progression.

163 activation of MAPK signaling, which promotes tumor invasion and progression.

164 s as a 3D physicotactic agent during sarcoma tumor invasion and propose the O2-controllable hydrogels

165 r and ErbB2 strongly implicated in mediating tumor invasion and spreading.

166 mine the role of endogenous c-Jun in mammary tumor invasion and stem cell function.

167 n lung squamous cell carcinoma and increases tumor invasion and survival through activation of focal

168 s, but absent in normal brain, that promotes tumor invasion and survival.

169 ure that invasive TAMs link angiogenesis and tumor invasion and that Wnt-signaling plays a role in me

170 that polysialic acid facilitates astrocytic tumor invasion and thereby tumor progression.

171 l periostin as an important mediator of ESCC tumor invasion and they indicate that organotypic (three

172 lass of matrix-degrading enzymes involved in tumor invasion and tissue remodeling, have yet to be lin

173 04D cells by RNA interference (RNAi) reduces tumor invasion and tumor growth.

174 elial cells and cooperate with Met to induce tumor invasion and vascularization.

175 se) proteins RhoA and RhoC are essential for tumor invasion and/or metastasis in breast carcinomas.

176 nase-9 (MMP-9) is associated with human lung tumor invasion and/or metastasis.

177 nd metastasis by stimulating cell migration, tumor invasion, and angiogenesis.

178 xenografts prevents in vivo SG formation and tumor invasion, and completely blocks lung metastasis in

179 aggressive human cancers, with rapid growth, tumor invasion, and development of distant metastases.

180 , cell migration, apoptotic-cell engulfment, tumor invasion, and HIV-1 infection, in diverse model sy

181 he astrogliotic capsule can directly inhibit tumor invasion, and its absence from GBM presents an env

182 gnaling directly regulates MMP-2 expression, tumor invasion, and metastasis, and that Stat3 activatio

183 ith downregulation of genes involved in EMT, tumor invasion, and metastasis.

184 on is considered critical in carcinogenesis, tumor invasion, and metastasis.

185 n is associated with increased angiogenesis, tumor invasion, and promotion of tumor cell resistance t

186 promoting cell growth, differentiation, and tumor invasion, and represent attractive targets for ant

187 hat N-cadherin expression is associated with tumor invasion, and that some cancer cells respond to sp

188 cy by increasing angiogenesis, tumor growth, tumor invasion, and tumor metastasis.

189 Tetraspanin CD82 suppresses cell migration, tumor invasion, and tumor metastasis.

190 olved in tumor cell survival, proliferation, tumor invasion, and/or immunosuppression.

191 ly inhibited tumor invasiveness in vitro and tumor invasion, angiogenesis, and metastasis in vivo.

192 lloproteinase-2 (MMP-2) has been linked with tumor invasion, angiogenesis, and metastasis.

193 tro, suggesting that the effects of SPDEF on tumor invasion are mediated, in part, through the suppre

194 ere the thickness of the lesion and depth of tumor invasion are the best prognostic indicators of cli

195 7 has previously been shown to inhibit local tumor invasion as well as lymph node and pulmonary metas

196 here an EMT-independent action of Snail1 on tumor invasion, as it is required for the activation of

197 on is important for therapeutic targeting of tumor invasion, as key regulatory pathways for intrinsic

198 vade an extracellular matrix, an established tumor invasion assay.

199 POE protein plays a significant role in OSCC tumor invasion because of its effects on cellular choles

200 ction inhibitors does not appreciably reduce tumor invasion, because these pathways are redundant; bl

201 chondrial dysfunction, stress signaling, and tumor invasion by a mechanism similar to that described

202 glutamate has also been found to facilitate tumor invasion by causing excitotoxic damage to normal b

203 tory signaling cascades in gliomas, blocking tumor invasion by directly targeting myosin II remains e

204 MMTV-TGF-alpha was the marked suppression of tumor invasion by DNIIR transgene expression.

205 is a potential tumor suppressor and inhibits tumor invasion by inducing suppressive cell microenviron

206 mechanism by which 14-3-3sigma guides breast tumor invasion by integrating cytoskeletal dynamics: it

207 Finally, TAMs can directly facilitate tumor invasion by recruiting tumor cells nearby vessels

208 TbetaRIII appeared to inhibit tumor invasion by undergoing ectodomain shedding and pro

209 rain but upregulated in gliomas and promotes tumor invasion by unknown mechanisms.

210 g mucosal resection techniques, the depth of tumor invasion can be established by histology, which al

211 al TGF-(beta)RII, whereas TGF-beta1-mediated tumor invasion cooperates with reduced TGF-(beta)RII sig

212 and heterogeneous and the regions of highest tumor invasion corresponded to areas of lowest pH.

213 Tumor invasion did not occur into regions with normal or

214 novel model where the EMT that occurs during tumor invasion downregulates tubulin tyrosine ligase, in

215 in vivo invasion; (2) that PTEN can inhibit tumor invasion even in the absence of its lipid phosphat

216 ar staining of pSTAT3-Y705 identified at the tumor invasion front in ductal breast carcinomas correla

217 The analysis of invading leader cells at the tumor invasion front is of significant interest as these

218 nal tumoroid culture which recapitulated the tumor invasion front, allowing for both quantification o

219 /ECM compositions, with a clearly demarcated tumor invasion front, thus allowing us to quantitatively

220 The acid-mediated tumor invasion hypothesis proposes altered glucose metab

221 Current models of this acid-mediated tumor invasion hypothesis, however, do not account for i

222 ER-negative breast cancer cells in vitro and tumor invasion in a co-transplant xenograft mouse model.

223 ing growth factor-beta1 (TGF-beta1) promotes tumor invasion in advanced squamous cell carcinomas, the

224 STAT3 was recently reported to suppress tumor invasion in Apc(min)(/+) mice.

225 mental tissue invasion for disc eversion and tumor invasion in Drosophila and modulate BM integrity w

226 results in significant inhibition of glioma tumor invasion in Matrigel and spheroid invasion assay m

227 ient PMo into Nr4a1-deficient mice prevented tumor invasion in the lung.

228 ix metalloproteinase-9 (MMP-9) in inhibiting tumor invasion in vitro and ex vivo.

229 n-regulation of LRP and inhibited astrocytic tumor invasion in vitro.

230 cantly decreased melanoma xenograft size and tumor invasion in vivo.

231 nd a candidate therapeutic target to inhibit tumor invasion in vivo.

232 egradation completely blocks both tissue and tumor invasion, indicating that modulation of BM is esse

233 diated activation of c-Src was important for tumor invasion induced by oncogenic Ras.

234 are not always surgically achievable due to tumor invasion into adjacent tissues or involvement of c

235 Tumor invasion into surrounding stromal tissue is a hall

236 Increased tumor invasion into the smooth muscle layer and aberrant

237 Tumor invasion is a critical step in the spread of cance

238 apability of human or murine CAFs to promote tumor invasion is dependent on Snail1 expression.

239 The effect of PEA-15 on tumor invasion is mediated by its interaction with ERK1/

240 of cell surface carbohydrates in astrocytic tumor invasion is not known.

241 sults demonstrate that the role of Snail1 in tumor invasion is not limited to EMT, but it is also dep

242 Collectively, our results demonstrate that tumor invasion is subject to polymorphic genetic control

243 Brain tumor invasion leads to recurrence and resistance to tre

244 dian survival included presence and depth of tumor invasion, margin-positive resection, and expressio

245 support the view that multiple mediators of tumor invasion may be important prognostic factor in gli

246 que opportunity to study the early events of tumor invasion, metastasis and drug responses.

247 expression of KLF8 and MMP9 with the patient tumor invasion, metastasis and poor survival.

248 Articles on tumor invasion, metastasis, and angiogenesis in normal a

249 trix metalloproteinases in the regulation of tumor invasion, metastasis, and angiogenesis was recogni

250 ose that encode for proteins associated with tumor invasion, metastasis, and angiogenesis.

251 nase-2 (COX-2) expression is associated with tumor invasion, metastasis, and poor prognosis in non-sm

252 andin E2 (PGE2)- and Akt/GSK-3beta-dependent tumor invasion/metastasis.

253 The acid-mediated tumor invasion model provides a simple mechanism linking

254 0.59, 0.80; P = .0004) for massive choroidal tumor invasion (n = 219).

255 motes tumor progression through induction of tumor invasion, neoangiogenesis, and immunosuppression.

256 Integrin beta3 is critical for tumor invasion, neoangiogenesis, and inflammation, makin

257 e 3-4 vs. grade 1; HR, 2.42; P < 0.001), and tumor invasion of adjacent structures (HR, 1.37; P < 0.0

258 Perineural tumor invasion of intrapancreatic nerves, neurogenic inf

259 gnificantly larger xenografts with increased tumor invasion of surrounding tissue in vivo.

260 ale sex, tumor site on the scalp or neck, or tumor invasion of the entire papillary dermis each indep

261 ry papillomatosis had progressive, bilateral tumor invasion of the lung parenchyma.

262 Tumor invasion of the otic capsule was associated with l

263 gies to identify and characterize markers of tumor invasion of the prostate capsule, an event general

264 carcinoma, may reflect tumor proximity to or tumor invasion of the pterygoid process.

265 In order to model tumor invasion of the stroma, we find it necessary to do

266 o-vasculature TKIs are delivered to decrease tumor invasion; on the other hand, the neo-vasculature c

267 y stage of tumor formation and contribute to tumor invasion once carcinomas have developed.

268 TEN is mechanistically involved in 'in vivo' tumor invasion or merely an epiphenomenon and, if the fo

269 idation set, RRM2B was negatively related to tumor invasion (OR = 0.45, 95% CI = 0.19-0.99, P = 0.040

270 most common etiology of cancer pain is local tumor invasion (primary or metastatic), involving inflam

271 brain metastases is not a surrogate of local tumor invasion, primary cancer type, or aggressive pheno

272 ession, are shared by both disc eversion and tumor invasion processes.

273 s correlated with elevated mTORC1 signaling, tumor invasion, progression, and poor prognosis.

274 ACTH secretion, cellular proliferation, and tumor invasion rates in vitro.

275 but the role of this receptor in astrocytic tumor invasion remains poorly understood.

276 he precise role and mechanism of Notch-1 for tumor invasion remains unclear.

277 er cell-intrinsic functions of CtsZ, whereas tumor invasion required contributions from both macropha

278 neoplasia in murine prostate and stimulated tumor invasion, similarly to ERG.

279 n is associated with increased angiogenesis, tumor invasion, suppression of host immunity and promote

280 Programmed cell death 4 (Pdcd4), a tumor invasion suppressor, is frequently downregulated i

281 rcellular adhesion and repulsion and acts as tumor/invasion suppressor in colorectal cancer.

282 , these data implicate Rap1GAP as a putative tumor/invasion suppressor in the thyroid.

283 ompared with surgical pathology for depth of tumor invasion (T).

284 racrine invasion loop, resulting in enhanced tumor invasion that is independent of macrophage signali

285 er of studies have implicated CD44 in breast tumor invasion, the evidence is still circumstantial.

286 most patients with T3 or T4 disease without tumor invasion through cartilage into soft tissues, a la

287 s found to have a critical role in promoting tumor invasion, through both macrophage and cancer cell

288 rrelates lymph node metastases with depth of tumor invasion, tumor size, presence of lymphovascular i

289 this study, we will investigate multispecies tumor invasion, tumor-induced angiogenesis, and focus on

290 ma driver whose levels can be tuned to favor tumor invasion, ultimately defining metastatic risk.

291 Tumor invasion was limited to the mucosa (T1a) in 75 pat

292 To further establish the role of PTEN in tumor invasion, we evaluated vector- and PTEN-transfecte

293 To analyze tumor invasion, we used O2-controllable hydrogels to rec

294 pecificity, and accuracy of MRI in detecting tumor invasion were determined.

295 Upfront resection and microvascular tumor invasion were poor prognostic factors for both OS

296 3 cm or more on histology, and microvascular tumor invasion were poor prognostic factors for OS and R

297 ist and the presence of LNM and the depth of tumor invasion were recorded.

298 s effective in cell-based in vitro models of tumor invasion, where it significantly abrogated invasio

299 -type PDGFRA decreases latency and increases tumor invasion, while ATRX knockdown is associated with

300 ment, during wound healing, and in cancerous tumor invasion, yet most detailed knowledge of cell migr